ArticlePharmacology research & perspectives2014
Mefloquine, an anti-malaria agent, causes reactive oxygen species-dependent cell death in mast cells via a secretory granule-mediated pathway.
Article in Pharmacology research & perspectives, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Mast cell proteases and their significance in physiology, pathology, and therapeutic approaches.Pharmacological reviews · 2026Review
- Role of mast cell-derived exosomes in exacerbating neuronal injury of experimental cerebral malaria.Parasites & vectors · 2025Article
- Monensin Suppresses Multiple Features of House Dust Mite-Induced Experimental Asthma in Mice.Inflammation · 2025Article
- Progress in the study of mefloquine as an antibiotic adjuvant for combination bacterial inhibition treatment.Frontiers in cellular and infection microbiology · 2024Review
- Mefloquine causes selective mast cell apoptosis in cutaneous mastocytosis lesions by a secretory granule-mediated pathway.Experimental dermatology · 2022Article
- Novel Strategies to Target Mast Cells in Disease.Journal of innate immunity · 2021Review
- Granule Leakage Induces Cell-Intrinsic, Granzyme B-Mediated Apoptosis in Mast Cells.Frontiers in cell and developmental biology · 2021Article
- T Helper Plasticity Is Orchestrated by STAT3, Bcl6, and Blimp-1 Balancing Pathology and Protection in Malaria.iScience · 2020Article
- Lysosome Inhibition by Mefloquine Preferentially Enhances the Cytotoxic Effects of Tyrosine Kinase Inhibitors in Blast Phase Chronic Myeloid Leukemia.Translational oncology · 2019Article
- Remodeling of secretory lysosomes during education tunes functional potential in NK cells.Nature communications · 2019Article
- Lysosomotropic challenge of mast cells causes intra-granular reactive oxygen species production.Cell death discovery · 2019Article
- Activation of Mast Cells PromoteFrontiers in cellular and infection microbiology · 2019Article
- Induction of Human Lung Mast Cell Apoptosis by Granule Permeabilization: A Novel Approach for Targeting Mast Cells.Frontiers in immunology · 2017Article
- Pharmacological treatment options for mast cell activation disease.Naunyn-Schmiedeberg's archives of pharmacology · 2016Review
- Mast cell activation in the skin of Plasmodium falciparum malaria patients.Malaria journal · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mast cells are known to have a detrimental impact on a variety of pathological conditions. There is therefore an urgent need of developing strategies that limit their harmful effects. The aim of this study was to accomplish this by developing a means of inducing mast cell apoptosis. The strategy was to identify novel compounds that induce mast cell apoptosis by permeabilization of their secretory lysosomes (granules). As a candidate, we assessed mefloquine, an anti-malarial drug that has been proposed to have lysosome-permeabilizing activity. Mefloquine was added to mast cells and administered in vivo, followed by assessment of the extent and mechanisms of mast cell death. Mefloquine was cytotoxic to murine and human mast cells. Mefloquine induced apoptotic cell death of wild-type mast cells whereas cells lacking the granule compounds serglycin proteoglycan or tryptase were shown to undergo necrotic cell death, the latter finding indicating a role of the mast cell granules in mefloquine-induced cell death. In support of this, mefloquine was shown to cause compromised granule integrity and to induce leakage of granule components into the cytosol. Mefloquine-induced cell death was refractory to caspase inhibitors but was completely abrogated by reactive oxygen species inhibition. These findings identify mefloquine as a novel anti-mast cell agent, which induces mast cell death through a granule-mediated pathway. Mefloquine may thus become useful in therapy aiming at limiting harmful effects of mast cells.
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